About: Microbial Neuraminidase Induces a Moderate and Transient Myelin Vacuolation Independent of Complement System Activation

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About: Microbial Neuraminidase Induces a Moderate and Transient Myelin Vacuolation Independent of Complement System Activation Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Microbial Neuraminidase Induces a Moderate and Transient Myelin Vacuolation Independent of Complement System Activation
Creator	Cifuentes, Manuel Fernández-Llebrez, Pedro Granados-Durán, Pablo Johnson, Krista Pérez-Martín, Margarita Hughes, Timothy Aureli, Massimo Del Mar Fernández-Arjona, María Dolores López-Ávalos, María Grondona, Jesús Hortobágyi, Tibor Morgan, B Szalardy, Levente
Source	Medline; PMC
abstract	AIMS: Some central nervous system pathogens express neuraminidase (NA) on their surfaces. In the rat brain, a single intracerebroventricular (ICV) injection of NA induces myelin vacuolation in axonal tracts. Here, we explore the nature, the time course, and the role of the complement system in this damage. METHODS: The spatiotemporal analysis of myelin vacuolation was performed by optical and electron microscopy. Myelin basic protein-positive area and oligodendrocyte transcription factor (Olig2)-positive cells were quantified in the damaged bundles. Neuronal death in the affected axonal tracts was assessed by Fluoro-Jade B and anti-caspase-3 staining. To evaluate the role of the complement, membrane attack complex (MAC) deposition on damaged bundles was analyzed using anti-C5b9. Rats ICV injected with the anaphylatoxin C5a were studied for myelin damage. In addition, NA-induced vacuolation was studied in rats with different degrees of complement inhibition: normal rats treated with anti-C5-blocking antibody and C6-deficient rats. RESULTS: The stria medullaris, the optic chiasm, and the fimbria were the most consistently damaged axonal tracts. Vacuolation peaked 7 days after NA injection and reverted by day 15. Olig2+ cell number in the damaged tracts was unaltered, and neurodegeneration associated with myelin alterations was not detected. MAC was absent on damaged axonal tracts, as revealed by C5b9 immunostaining. Rats ICV injected with the anaphylatoxin C5a displayed no myelin injury. When the complement system was experimentally or constitutively inhibited, NA-induced myelin vacuolation was similar to that observed in normal rats. CONCLUSION: Microbial NA induces a moderate and transient myelin vacuolation that is not caused either by neuroinflammation or complement system activation.
has issue date	2017-03-07(xsd:dateTime)
bibo:doi	10.3389/fneur.2017.00078
bibo:pmid	28326060
has license	cc-by
sha1sum (hex)	5fb0184e30b9a7107983d9316b1c925508b75834
schema:url	https://doi.org/10.3389/fneur.2017.00078
resource representing a document's title	Microbial Neuraminidase Induces a Moderate and Transient Myelin Vacuolation Independent of Complement System Activation
has PubMed Central identifier	PMC5339270
has PubMed identifier	28326060
schema:publication	Front Neurol
resource representing a document's body	covid:5fb0184e30b9a7107983d9316b1c925508b75834#body_text
is schema:about of	named entity 'MICROBIAL' named entity 'axonal' named entity 'complement system' named entity 'Transient' named entity 'Myelin' named entity 'VACUOLATION' named entity 'EXPRESS' named entity 'THEIR' named entity 'CENTRAL NERVOUS SYSTEM' named entity 'TRANSIENT' named entity 'MYELIN' named entity 'NEURAMINIDASE' named entity 'COMPLEMENT SYSTEM' named entity 'AXONAL' named entity 'MYELIN' named entity 'INDEPENDENT OF' named entity 'ACTIVATION' named entity 'MODERATE' named entity 'AIMS' named entity 'SINGLE' named entity 'COMPLEMENT SYSTEM' named entity 'SURFACES' named entity 'NEURAMINIDASE' named entity 'VACUOLATION' named entity 'TRACTS' named entity 'DAMAGE' named entity 'INJECTION' named entity 'NATURE' named entity 'HERE' named entity 'RAT BRAIN' named entity 'ROLE' named entity 'TIME COURSE' named entity 'PATHOGENS' covid:arg/5fb0184e30b9a7107983d9316b1c925508b75834 named entity 'time' named entity 'myelin' named entity 'central nervous system' named entity 'complement system' named entity 'pathogens' named entity 'complement' named entity 'Microbial' named entity 'meninges' named entity 'vacuolation' named entity 'frontal cortex' named entity 'antibody' named entity 'myelin' named entity 'ipsilateral' named entity 'Universidad de Málaga' named entity 'myelin sheaths' named entity 'vacuoles' named entity 'myelin' named entity 'vacuolation' named entity 'C5a' named entity 'MAG' named entity 'complement-mediated' named entity 'apoptosis' named entity 'tribromoethanol' named entity 'periventricular' named entity 'positive control' named entity 'CSF' named entity 'immunolocalization' named entity 'demyelination' named entity 'MAG' named entity 'fluorescent staining' named entity 'vacuolated' named entity 'ventricle' named entity 'myelin' named entity 'quantitative method' named entity 'stereotaxic surgery'

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